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PubMed2004

The Janus face of inflammation in ischemic brain injury.

Brain ischemia elicits an intense inflammatory reaction as evidenced by endogenous activation of microglia and infiltration of leukocytes from the systemic circulation into the brain. A key issue regarding the well-described inflammation in brain injury is whether this reaction is of salutary or detrimental nature in the short and longterm post ischemia. In this brief review, evidence in support for the possible beneficial as well as detrimental role of inflammatory cells and mediators in ischemic brain injury is highlighted. We offer the opinion that both benefits and adverse effects of the inflammatory reaction at large depent on the levels of a specific mediator, the temporal relationships to the injury, the context in which the mediator operates and the spatial relationships to the injury.

Animals↗

PubMed1993

[Brain injury and brain disease. Need and importance of early rehabilitation].

Early rehabilitation means rehabilitation which begins during the treatment for acute illness or trauma, immediately after the management of life-threatening conditions and stabilization of vital functions. Early rehabilitation is intended to make extensive use of the regenerative capacities of the brain and prepare effortless transition to further training programs. The necessity of early rehabilitation after severe brain injury or vascular brain disease is now recognized. However the means available now, i.e. trained staff, equipment and buildings, are insufficient. In order to estimate the resources needed the epidemiology of head and brain injury and vascular brain disease in Germany was analyzed by Infratest Gesundheitsforschung, Munich. The study was initiated and supported by the Kuratorium ZNS. The data concerning the years spanning 1987 to 1989 and the emerging conclusions will be presented. Also, important and meanwhile accepted suggestions for the founding and equipment of rehabilitative care units will be discussed.

Brain Damage, Chronic↗

PubMed2006

[Cerebral metabolism and brain injury].

Brain energy metabolism and signal transduction are intimely intricated. At the cellular level this is reflected by the interdependent metabolism of glutamate and glucose and the energetic compartmentalization between astrocytic glycolysis and neuronal metabolism. Astrocytes appear to have a particular importance in brain metabolism by regulating microcirculation and the repartition of energetic substrates in function of synaptic activity. The high level of O(2) consumption compared to the mass of tissue confers a particular vulnerability of brain to oxidative stress. The synthesis of glutathione, the main anti-oxidant of brain, appears to be dependent of the regulation of synaptic glutamate concentration by astrocytes. Deficiencies of astrocytes functions appear to play a key role in the physiopathology of brain injury.

Animals↗

PubMed1992

Intracellular acidosis in human and experimental brain injury.

Brain tissue acidosis is considered to play a role in the complex sequence of events following traumatic brain injury. This report reviews the experimental and clinical research conducted at the Medical College of Virginia to help clarify the extent of metabolic derangement that occurs and to evaluate the effect of treatment. Experimental injury models in ventilated animals showed that trauma produces a mild brain tissue acidosis that recovers within hours of injury. Hypoxia combined with trauma produces a relative ischemia and exacerbates the acidosis, which eventually resolves with resuscitation. Other studies revealed that CSF lactate measurements should be interpreted with caution, particularly in patients with subarachnoid hemorrhage. The results of two randomized clinical trials testing therapeutic effects of sustained hyperventilation and treatment with tromethamine (THAM) are discussed.

Acidosis↗

PubMed2005

Sulforaphane enhances aquaporin-4 expression and decreases cerebral edema following traumatic brain injury.

Brain edema, the infiltration and accumulation of excess fluid causing an increase in brain tissue volume, often leads to a rise in intracranial pressure and is a key contributor to the morbidity and mortality associated with traumatic brain injury (TBI). The cellular and molecular mechanisms contributing to the development/resolution of TBI-associated brain edema are poorly understood. Aquaporin-4 (AQP4) water channel is expressed at high levels in brain astrocytes, and the bidirectional transport of water through these channels is critical for the maintenance of brain water homeostasis. By using a rodent injury model, we show that TBI decreased AQP4 level in the injury core and modestly increased it in the penumbra region surrounding the core. Postinjury administration of sulforaphane (SUL), an isothiocyanate present in abundance in cruciferous vegetables such as broccoli, attenuated AQP4 loss in the injury core and further increased AQP4 levels in the penumbra region compared with injured animals receiving vehicle. These increases in AQP4 levels were accompanied by a significant reduction in brain edema (assessed by percentage water content) at 3 days postinjury. These findings suggest that the reduction of brain edema in response to SUL administration could be due, in part, to water clearance by AQP4 from the injured brain.

Animals↗

PubMed2006

Specificity and divergence in the neurobiologic effects of different metallothioneins after brain injury.

Brain injury and neuroinflammation are pathophysiologic contributors to acute and chronic neurologic disorders, which are progressive diseases not fully understood. Mammalian metallothioneins I and II (MT-I&II) have significant neuroprotective functions, but the precise mechanisms underlying these effects are still unknown. To gain insight in this regard, we have evaluated whether a distant, most likely single-domain MT (Drosophila MTN) functions similarly to mammalian MT-I&II (recombinant mouse MT-I and human MT-IIa and native rabbit MT-II) after cryogenic injury to the cortex in Mt1&2 KO mice. All the recombinant proteins showed similar neuroprotective properties to native MT-II, significantly reducing brain inflammation (macrophages, T cells, and pro-inflammatory cytokines), oxidative stress, neurodegeneration, and apoptosis. These results in principle do not support specific protein-protein interactions as the mechanism underlying the neuroprotective effects of these proteins because a non-homologous and structurally unrelated MT such as Drosophila MTN functions similarly to mammalian MTs. We have also evaluated for the first time the neurobiologic effects of exogenous MT-III, a major CNS MT isoform. Human rMT-III, in contrast to human nMT-IIa, did not affect inflammation, oxidative stress, and apoptosis, and showed opposite effects on several growth factors, neurotrophins, and markers of synaptic growth and plasticity. Our data thus highlight specific and divergent roles of exogenous MT-III vs. the MT-I&II isoforms that are consistent with those attributed to the endogenous proteins, and confirm the suitability of recombinant synthesis for future therapeutic use that may become relevant to clinical neurology.

Analysis of Variance↗

PubMed2006

Continuous assessment of cerebrovascular autoregulation after traumatic brain injury using brain tissue oxygen pressure reactivity.

OBJECTIVE: To evaluate whether two newly developed indexes of brain tissue oxygen pressure reactivity (ORx and bPtio2) provide information on the status of cerebrovascular autoregulation after traumatic brain injury. This was accomplished by analyzing the relationship between these indexes and an index of cerebrovascular pressure reactivity (PRx). PRx is an established parameter for estimation of cerebrovascular autoregulation. DESIGN: Retrospective analysis of prospectively collected data. SETTING: Neurosurgical intensive care unit of a university hospital. PATIENTS: Twenty-seven patients suffering from severe traumatic brain injury. INTERVENTIONS: Continuous monitoring of mean arterial blood pressure, intracranial pressure, cerebral perfusion pressure, and partial pressure of brain tissue oxygen (Ptio2) was performed for an average of 6.5 days. ORx was calculated as a moving correlation coefficient between values of cerebral perfusion pressure and Ptio2. The bPtio2 was calculated as a moving value of the slope of the linear regression function between cerebral perfusion pressure and Ptio2. PRx was calculated as a moving correlation coefficient between values for intracranial pressure and mean arterial blood pressure. Outcome was assessed at 6 months after traumatic brain injury (Glasgow Outcome Scale). MEASUREMENTS AND MAIN RESULTS: Both ORx and bPtio2 correlated significantly with PRx (r=.55 for ORx, r=.52 for bPtio2, p<.01). PRx and ORx showed a significantly negative correlation to the monitored Ptio2 values (r=-.42 for PRx, r=-.41 for ORx, p<.05) and outcome (r=-.52 for PRx, r=-.62 for ORx, p<.01), whereas bPtio2 did not. CONCLUSIONS: ORx and, to a lesser extent, bPtio2 correlated with the autoregulatory marker PRx and provide additional information about the status of cerebrovascular autoregulation after traumatic brain injury. The data also suggested that patients with impaired autoregulation are at increased risk for secondary cerebral hypoxia.

Adolescent↗

PubMed1999

Paradoxical facilitation of a free recall of nonwords in persons with traumatic brain injury.

Brain damage is usually associated with behavioral deficits. However, there is an increasing amount of evidence that lesions of some brain regions are associated with improvements instead of impairments of certain behaviors. We report the results of a study of free recall performance in subjects with traumatic brain injury. One-fourth of the subjects displayed above-normal performance in recall of nonwords. No such facilitation was found with nine lists of words.

Adolescent↗

PubMed2006

Mechanisms of neural plasticity following brain injury.

Brain insults cause rapid cell death, and a disruption of functional circuits, in the affected regions. As the injured tissue recovers from events associated with cell death, regenerative processes are activated that over months lead to a certain degree of functional recovery. Factors produced by new neurons and glia, axonal sprouting of surviving neurons, and new synapse formation help to re-establish some of the lost functions. The timing and location of such events is crucial in the success of the regenerative process. Comprehensive gene expression profiling and proteomic analyses have enabled a deeper molecular and cellular mechanistic understanding of post-injury brain regeneration. These new mechanistic insights are aiding the design of novel therapeutic modalities that enhance regeneration.

Animals↗

PubMed1999

Early and late posttraumatic seizures in traumatic brain injury rehabilitation patients: brain injury factors causing late seizures and influence of seizures on long-term outcome.

PURPOSE: To demonstrate risk factors involved in the origin of late posttraumatic seizures (LPTSs) in civilian traumatic brain injury (TBI) rehabilitation patients and the occurrence of LPTSs in this population, as well as the time of the first late seizures, and influence of these seizures on functional and occupational long-term outcome. METHODS: A consecutive sample of 490 patients (age range, 0.8-71 years) with TBI, and with postinjury problems in their education and employment, were followed up for > or =5 years from the time of injury in a rehabilitation and reemployment program. The study was carried out at the outpatient neurologic clinic of the Kauniala Hospital, which specializes in brain injuries in Finland and works in close cooperation with the Department of Clinical Neurosciences at the Helsinki University Central Hospital. Main outcome measures were functional outcome, as measured on the Glasgow Outcome Scale (GOS), and the capacity for employment at the end of follow-up. Outcomes were studied separately among patients with late seizures and for the nonseizure group. RESULTS: Children age 7 years or younger at time of injury more often had early posttraumatic seizures (EPTSs), than did adolescents or adults. The time elapsed between brain injury and the first late seizure also was longer in older age groups. EPTSs and depressed skull fracture had a statistically significant relation to the origin of LPTSs. Permanent posttraumatic neurologic deficit, linear skull fracture, and permanent local brain lesion documented on a computed tomography (CT) scan appeared clinically important as risk factors. Late seizures did worsen the functional outcome but had no significant influence on reemployment at the end of follow-up. CONCLUSIONS: Young children are more prone to early seizures, and adolescents and adults, to late seizures. The main risk factors for LPTSs are early seizures and depressed skull fracture. Severity of brain injury, as measured by a low GCS score, prolonged unconsciousness, and posttraumatic amnesia (PTA) without local brain lesion, should not be considered risk factor for LPTSs. Thorough follow-up of patients with TBI with seizures and adequate antiepileptic therapy may help attain rehabilitation goals and reemployment.

Adolescent↗

PubMed1989

The role of excitatory amino acids and NMDA receptors in traumatic brain injury.

Brain injury induced by fluid percussion in rats caused a marked elevation in extracellular glutamate and aspartate adjacent to the trauma site. This increase in excitatory amino acids was related to the severity of the injury and was associated with a reduction in cellular bioenergetic state and intracellular free magnesium. Treatment with the noncompetitive N-methyl-D-aspartate (NMDA) antagonist dextrophan or the competitive antagonist 3-(2-carboxypiperazin-4-yl)propyl-1-phosphonic acid limited the resultant neurological dysfunction; dextrorphan treatment also improved the bioenergetic state after trauma and increased the intracellular free magnesium. Thus, excitatory amino acids contribute to delayed tissue damage after brain trauma; NMDA antagonists may be of benefit in treating acute head injury.

Animals↗

PubMedDate not supplied

Early self-awareness following traumatic brain injury: comparison of brain injury and orthopedic inpatients using the Functional Self-Assessment Scale (FSAS).

OBJECTIVE: To examine the Functional Self-Assessment Scale (FSAS) in hospitalized orthopedic patients with no brain dysfunction, and compare results to prior self-awareness data collected with brain injury patients. DESIGN: Comparison of patient and staff ratings on FSAS using paired sample t tests. PARTICIPANTS: Thirty-one adult volunteers hospitalized on National Rehabilitation Hospital (NRH) orthopedic treatment unit. MEASURES: FSAS was used to compare patient and staff ratings of patient performance on tasks relevant for inpatient rehabilitation. Subjects were screened to rule out brain impairment. RESULTS: Statistically significant but very small differences were found between orthopedic patients and therapist ratings using the FSAS. However, brain injury patients' ratings show a significantly larger discrepancy between self-therapist ratings than do orthopedic patients. CONCLUSION: Impaired self-awareness is related to brain injury rather than nonspecific factors in rehabilitation inpatients.

Adolescent↗

PubMed1988

Experimental traumatic brain injury elevates brain prostaglandin E2 and thromboxane B2 levels in rats.

Prostaglandin E2 (PGE2) and thromboxane B2 (TxB2) levels were measured in rats following experimental traumatic brain injury. Rats (n = 36) were prepared for fluid percussion brain injury under pentobarbital anesthesia. Twenty-four hours later, rats were lightly anesthetized using methoxyflurane, injured (2.3 atm), and killed 5 or 15 min later. Twelve of the rats died before and are not included in the analyses. The following groups were used for data analysis: group I (n = 6) were sham-injured rats prepared for injury but not injured: group II (n = 6) were injured and killed 5 min later; group III (n = 12) were injured and killed 15 min posttrauma. Thirty seconds prior to sacrifice by decapitation into liquid nitrogen, all rats were injected with indomethacin (3 mg/kg, intravenously [IV]) to prevent postmortem PG synthesis. After sacrifice, brains were removed, weighed, and homogenized in a small quantity of phosphate buffer with indomethacin (50 micrograms/ml). PGE2 and TxB2 levels were determined using double-label radioimmunoassays. Posttraumatic convulsions were observed in 5 of 12 rats in group III and these rats were analyzed separately. PGE2 and TxB2 levels increased significantly (p less than 0.05) in both hemisphere and brainstem 5 min posttrauma. Fifteen minutes after injury, both PGE2 and TxB2 levels remained elevated but the levels were lower than at 5 min in the rats that did not exhibit posttraumatic seizures. This decrease in PG levels at 15 min was not observed in the rats that had seizures after injury and both PGE2 and TxB2 levels remained high in hemispheres and brainstem. Thus, fluid percussion brain injury results in substantial elevations in PGE2 and TxB2 levels and posttraumatic seizures exacerbate the observed increases.

Animals↗

PubMed1998

Construct validation of the Hoensbroeck Disability Scale for Brain Injury in acquired brain injury rehabilitation.

PURPOSE: To evaluate the construct validity of the Hoensbroeck Disability Scale for Brain Injury (HDSB) against the Disability Rating Scale (DRS). METHODS: The HDSB was correlated with the DRS at admission, 6 weeks later and at discharge in 33 brain injured patients during post-acute rehabilitation. Next, to study the longitudinal construct validity of the HDSB the mean changes in score of the HDSB and the DRS were correlated. Finally, the sensitivity to change over a 6-week period was evaluated by comparison of the effect sizes of the HDSB scores with the DRS scores. RESULTS: The HDSB subscales correlate high and in the expected direction with the DRS at all three points in time. The correlation of the changes between HDSB and DRS is moderate, but in the expected direction. The sensitivity to change in time of the HDSB is lower than that of the DRS. CONCLUSIONS: This study supports the validity of the HDSB as an instrument to describe the disability of acquired brain injury patients at a single point in time. Its ability to measure changes in disability over time is questionable and needs further investigation.

Activities of Daily Living↗

PubMed1993

A review of brain retraction and recommendations for minimizing intraoperative brain injury.

Brain retraction is required for adequate exposure during many intracranial procedures. The incidence of contusion or infarction from overzealous brain retraction is probably 10% in cranial base procedures and 5% in intracranial aneurysm procedures. The literature on brain retraction injury is reviewed, with particular attention to the use of intermittent retraction. Intraoperative monitoring techniques--brain electrical activity, cerebral blood flow, and brain retraction pressure--are evaluated. Various intraoperative interventions--anesthetic agents, positioning, cerebrospinal fluid drainage, operative approaches involving bone resection or osteotomy, hyperventilation, induced hypotension, induced hypertension, mannitol, and nimodipine--are assessed with regard to their effects on brain retraction. Because brain retraction injury, like other forms of focal cerebral ischemia, is multifactorial in its origins, a multifaceted approach probably will be most advantageous in minimizing retraction injury. Recommendations for operative management of cases involving significant brain retraction are made. These recommendations optimize the following goals: anesthesia and metabolic depression, improvement in cerebral blood flow and calcium channel blockade, intraoperative monitoring, and operative exposure and retraction efficacy. Through a combination of judicious retraction, appropriate anesthetic and pharmacological management, and aggressive intraoperative monitoring, brain retraction should become a much less common source of morbidity in the future.

Adrenal Cortex Hormones↗

PubMed2005

Elevated lactate as an early marker of brain injury in inflicted traumatic brain injury.

BACKGROUND: Traumatic brain injury is a major cause of disability and death in the pediatric population. The metabolic and neurochemical abnormalities that underlie traumatic brain injury remain poorly understood, but hypoxia-ischemic injury might play an important role. OBJECTIVE: This study evaluated children with inflicted traumatic brain injury using magnetic resonance spectroscopy (MRS). We postulated that children with hypoxic-ischemic injury indicated by elevated lactate in the acute phase of injury will have worse early neurological status and short-term clinical outcomes than those without lactate upon MRS. MATERIALS AND METHODS: This prospective study employed proton MRS to sample bilaterally the frontal lobes and the parasagittal cortex within the parietal and occipital lobes of 11 patients with inflicted traumatic brain injury who were undergoing a clinical MRI examination. Patients' measured clinical course while hospitalized included initial neurological evaluation, presence of seizure activity, need for admission to the pediatric intensive care unit (PICU), number of days hospitalized, presence of retinal hemorrhages and presence of bone fractures. Measurement of outcome was determined using the Pediatric Overall Performance Category Scale (POPCS; 1=good performance; 6=death). RESULTS: Four children demonstrated elevated lactate and diminished N-acetyl aspartate (a neuronal marker) within several regions, indicating global ischemic injury (lactate-positive global group). These four children all had seizure activity and abnormal initial neurological examinations and required admission to the PICU. The mean POPCS for this group was 3.25. In four other children, lactate was detected within at least one region, indicating a focal ischemic injury (lactate-positive focal group); two of these children had seizure activity, and two had an abnormal initial neurological examination. The mean POPCS score was 1.5 for this group. The remaining three children had no evidence of lactate upon MRS (lactate-negative group). These children did not have seizure activity, did not require admission to the PICU, nor did they have initial abnormal neurological examinations. The mean POPCS score was 1.3 for this group. SUMMARY: Patients with inflicted traumatic brain injury and evidence of hypoxic-ischemic injury as indicated by elevated lactate on MRS tend to have worse early neurological status and early outcome scores. Lactate levels as sampled by MRS might predict early clinical outcome in inflicted traumatic brain injury.

Aspartic Acid↗

PubMed2004

Voluntary exercise following traumatic brain injury: brain-derived neurotrophic factor upregulation and recovery of function.

Voluntary exercise leads to an upregulation of brain-derived neurotrophic factor (BDNF) and associated proteins involved in synaptic function. Activity-induced enhancement of neuroplasticity may be considered for the treatment of traumatic brain injury (TBI). Given that during the first postinjury week the brain is undergoing dynamic restorative processes and energetic changes that may influence the outcome of exercise, we evaluated the effects of acute and delayed exercise following experimental TBI. Male Sprague-Dawley rats underwent either sham or lateral fluid-percussion injury (FPI) and were housed with or without access to a running wheel (RW) from postinjury days 0-6 (acute) or 14-20 (delayed). FPI alone resulted in significantly elevated levels of hippocampal phosphorylated synapsin I and phosphorylated cyclic AMP response element-binding-protein (CREB) at postinjury day 7, of which phosphorylated CREB remained elevated at postinjury day 21. Sham and delayed FPI-RW rats showed increased levels of BDNF, following exercise. Exercise also increased phosphorylated synapsin I and CREB in sham rats. In contrast to shams, the acutely exercised FPI rats failed to show activity-dependent BDNF upregulation and had significant decreases of phosphorylated synapsin I and total CREB. Additional rats were cognitively assessed (learning acquisition and memory) by utilizing the Morris water maze after acute or delayed RW exposure. Shams and delayed FPI-RW animals benefited from exercise, as indicated by a significant decrease in the number of trials to criterion (ability to locate the platform in 7 s or less for four consecutive trials), compared with the delayed FPI-sedentary rats. In contrast, cognitive performance in the acute FPI-RW rats was significantly impaired compared with all the other groups. These results suggest that voluntary exercise can endogenously upregulate BDNF and enhance recovery when it is delayed after TBI. However, when exercise is administered to soon after TBI, the molecular response to exercise is disrupted and recovery may be delayed.

Animals↗

PubMed2001

Sustained, long-lasting inhibition of nitric oxide synthase aggravates the neural damage in some models of excitotoxic brain injury.

Brain nitric oxide (NO) can be a mediator of physiological and neuroprotective actions and an effector of neural damage. The effectiveness of acute or chronic inhibition of NO production in in vivo experiments of neurotoxicity/neuroprotection is controversial. We report here on the effects of a chronic, sustained inhibition of nitric oxide synthase (NOS) on the neurodegenerative damage caused by three different excitotoxic lesions. The damage caused by intrastriatal injection of ibotenic or kainic acid was aggravated in rats subjected to chronic NOS inhibition. On the contrary, the drop of cortical cholinergic input consequent to ibotenic acid-mediated degeneration of basal forebrain neurons was not altered by chronic NOS inhibition. The worsening of the damage was not related to any overt differential sensitivity to excitotoxicity of NOS-containing striatal neurons under conditions of NOS inhibition. These results suggest that, contrary to what has been often reported for short-term, mild inhibition of NO production, chronic and sustained NOS inhibition may exacerbate neuropathology. Thus, long-lasting shortage of NO may be detrimental when neuroprotective mechanisms related to the physiological action of this free radical are severely impaired. Although we cannot exclude that inhibition of the endothelial NOS isoform could have contributed to the worsening of neuropathology, differences among the paradigms of neurotoxicity used in the present study suggest a primary involvement of the neuronal NOS isoform. In view of the potential therapeutic use of NOS inhibitors, the effects of a too drastic alteration of the balance between neuroprotective and neurodegenerative actions of NO should be carefully considered.

Animals↗